Saccular intracranial aneurysms are characterized by marked thinning of the vessel wall at the site of the out-pouching. Thinning typically occurs at branch points of the intracranial vessels, particularly upon the circle of Willis. Such lesions are found in about 3 per cent of individuals examined at autopsy. Although many aneurysms never rupture, ruptured intracranial aneurysms account for 28 000 subarachnoid haemorrhages each year in the United States of America.

Patients with a symptomatic intracranial aneurysm most commonly present with subarachnoid haemorrhage. Bleeding is signalled by severe headache of sudden onset, which may be accompanied by progressive neurological symptoms and signs, such as hemiparesis. Some patients may progress to coma. Occasionally aneurysms cause manifestations due to their mass effect, or may be associated with seizures or transient ischaemic attacks.

Complications often follow a subarachnoid haemorrhage. The most common complication is rebleeding, which occurs in 4 per cent of patients within the first 24 h, and in 19 per cent within the first 2 weeks of a haemorrhage. Such rebleeding is often more serious than the initial event, particularly if there have been multiple previous haemorrhages. Symptomatic disturbance due to cerebrovascular vasospasm occurs in about one-third of patients. These develop delayed onset focal neurological symptoms, which may progress to cause serious deficit or death. Hydrocephalus may also occur. Disturbances of electrolyte balance and cardiac function may result in arrhythmias and myocardial infarction.

Clinical assessment includes the assignment of a clinical grade, according to the system of Hunt and Hess. Patients designated grade 1 or 2 are in good neurological condition; those classed as grade 3 show drowsiness or significant focal signs, while grade 4 and 5 patients are severely affected. The use of this type of grading system, in concert with the Glasgow coma scale, is useful in the repeated evaluation of patients and the assessment of results. It also provides data which are useful in determining the timing of intervention.

All patients should be investigated by CT scanning. In the rare event when CT does not demonstrate subarachnoid bleeding, spinal puncture can be used to confirm the diagnosis. The CT scan will also document the presence of hydrocephalus, cerebral infarction, and other complications. Four-vessel cerebral angiography should be performed unless the patient is moribund. Arteriography demonstrates the aneurysm, its neck, and its relationship with parent and branch vessels. It will also reveal the presence of multiple aneurysms, which are present in 15 per cent of patients. No bleeding site can be identified in 15 per cent of patients: repeat angiography performed 2 weeks later may allow identification of the bleeding point.

MRI may be helpful in identifying the site of haemorrhage, demonstrating mural thrombus, or depicting the relationship of the aneurysm to cerebral structures. Magnetic resonance angiography is sometimes used. Transcranial Doppler examination may provide valuable information about blood flow through major vessels, and is particularly useful in the bedside monitoring of patients with cerebral vasospasm. Studies of cerebral blood flow are used for research purposes, but have little clinical application.

Medical therapy includes primarily bed rest and application of pneumatic boots to prevent pulmonary embolism. If deep vein thrombosis occurs, immediate angiography is indicated with insertion of a vena cava filter to prevent a potentially fatal pulmonary embolus. Hypervolaemic haemodilution is warranted to prevent cerebral vasospasm, except in patients with cardiac failure.

Antihypertensive drugs should be administered to keep blood pressure at a normal level: administration of nimodipine has been shown to decrease the risk of neurological deficit and death in patients with subarachnoid haemorrhage. Phenytoin may also be administered if convulsions develop, and sedatives and stool softeners should be administered as needed. Corticosteroid treatment is appropriate in patients with neurological deficits, signs of increased intracranial tension, or severe headache. Antifibrinolytic therapy should only be administered to those who are not scheduled to undergo early surgical or embolic treatment.

Vasospasm is treated by hypervolaemic haemodilution and induction of hypertension by administration of neosynephrine or dopamine; administration of mannitol is useful in symptomatic patients. Pulmonary artery and radial artery pressures must be carefully monitored during such therapy. If neurological function continues to decline despite medical therapy, angioplasty may be required. The use of tissue plasminogen activator to lyse the subarachnoid clot and lazeroids to prevent cerebral infarction are currently areas of research.

Ventriculostomy is indicated as an emergency procedure in patients with grade 4 or 5 disease, or in those showing progressive decline and hydrocephalus. The intracranial pressure should be lowered gradually since an abrupt increase in transmural pressure may cause recurrent haemorrhage.

Craniotomy may also be required as an emergency procedure. This is indicated in patients with progressive neurological deterioration due to the presence of intracerebral haematoma. Craniotomy may also be performed to prevent a potentially fatal rebleed. Early operation is particularly beneficial in patients classed as grades 1 to 3, who have accessible aneurysms. A few patients, particularly those in whom the lesion is situated in the posterior fossa, benefit more from surgery undertaken after about 2 weeks, when cerebral swelling has abated.

Modern neuroanaesthetic techniques allow gentle intubation without a hypertensive response. This, combined with hyperventilation and osmotherapy to relax the brain, allows the aneurysm obliteration by microsurgery. Clipping is the best method for most patients, and intraoperative angiography allows adjustment of clips to ensure their optimal positioning, confirming the complete obliteration of the aneurysm with no compromise of parent vessels. Although many factors affect the outcome, experienced teams can produce good or excellent results in 80 per cent of patients undergoing early surgery, with a mortality rate of less than 10 per cent.

Endovascular treatment with intraluminal obliteration of the aneurysm may be used in patients who are medically unfit for surgery, and in those whose aneurysm is considered to be inoperable. Although being used quite widely in these situations, it is still to early for a final evaluation of this approach to aneurysm treatment.

About 5 per cent of intracerebral aneurysms are classed as giant (more than 25 mm in diameter). These lesions can cause a mass effect or seizures, or may present with subarachnoid haemorrhage. CT and MRI are useful in the assessment of these aneurysms. Many of these lesions can be treated by clipping; in some cases occlusion of the parent vessel may be the best approach. If this is the case, a test occlusion, performed with the patient awake, will indicate whether a bypass graft will be required to prevent cerebral ischaemia after such therapy.

CT or MRI performed for the assessment of vague symptoms or minor head injury may reveal the presence of an unruptured aneurysm. Those 10 mm or more in diameter have a high incidence of rupture, and their obliteration is indicated in most patients. The indications for treatment of smaller lesions are less clear. The decision of whether or not to operate should be based upon the patient's age, general medical condition, the location of the aneurysm, and the experience of the surgeon: a morbidity rate of less than 5 per cent can be achieved in these patients. Multiple aneurysms, which account for 15 per cent of all intracranial aneurysms, tend to rupture at a smaller size. Repeated angiography after 12 months may be indicated if lesions are less than 5 mm in diameter, or if they are located in areas which are difficult to reach at surgery.

Infectious aneurysms occur in 4 to 10 per cent of patients with subacute endocarditis, and they may cause subarachnoid haemorrhage or cerebral infarction. Such aneurysms frequently occur on the distal intracranial vasculature: their size and location can be documented by angiography. Administration of a 3- to 6-week course of antibiotics active against the causative organism are often effective. If repeat angiography shows the lesion to have increased in size despite such therapy, surgical excision is warranted.

Traumatic aneurysms are uncommon following closed head injury, but are more likely to occur after a penetrating injury. If cerebral angiography reveals an aneurysm, prompt operation is indicated or repeat angiography for deep lesions: surgical excision is indicated if the lesion has increased in size. Prompt surgery should be undertaken if a traumatic aneurysm is associated with subarachnoid haemorrhage.

Patients who have undergone treatment for intracranial aneurysm require careful, life-long monitoring due to the possibility of recurrence. Postoperative angiography should be performed to confirm that the lesion has been completely obliterated. If the examination reveals any irregularity in the contour of the vessel, regular repeat angiography is indicated, and reoperation may be necessary. Enlargement of such an irregularity should prompt careful consideration of the need for reoperation to prevent recurrence of a subarachnoid haemorrhage.

Ojemann RG, Heros RC, Crowell RM. Surgical Management of Cerebrovascular Diseases, 2nd edn. Baltimore: Williams and Wilkins, 1988.

Weir B. Aneurysms Affecting the Nervous System. Baltimore: Williams and Wilkins, 1987.